LINC00261 is downregulated in endometrial carcinoma and associated with metastasis of this cancer. LINC00261 elevates FOXO1 protein levels through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion.

PurposeThis study is aimed to investigate the specific regulatory role of S100 calcium binding protein A11 (S100A11) on cervical cancer (CC), and reveal the potential mechanisms relating to Wnt/β-catenin signaling.Patients and methodsThe expression of S100A11 in cervical squamous cell carcinoma (CSCC), adjacent non-cancerous, cervical intraepithelial neoplasia (CIN), and normal cervical tissues was detected by quantitative real-time PCR and/or immunohistochemistry. After transfection of pENTER-S100A11 or sh-S100A11-1/sh-S100A11-2, the viability, cell cycle, migration and invasion of C33A or SiHa cells were detected. The tumor volume and tumor weight were measured after injection of transfected C33A cells into mice. The expression of E-caherin (CDH2), N-caherin (CDH1), β-catenin (CTNNB1), and c-Myc (MYC) in C33A and SiHa cells was detected by Western blot.ResultsThe expression of S100A11 was significantly higher in CSCC tissues than in adjacent non-cancerous, CIN, and normal cervical tissues (P < 0.05). S100A11 expression was positively correlated with the FIGO stage and lymph node metastasis of CSCC patients (P < 0.05). The transfection of pENTER-S100A11 into C33A cells significantly increased the cell viability, the percentage of cells in G2/M phase, the numbers of migratory and invasive cells, as well as the tumor volume and weight in mice (P < 0.05). Overexpression of S100A11 also significantly downregulated E-caherin, and upregulated N-caherin, β-catenin, and c-Myc in C33A cells (P < 0.05). The transfection of sh-S100A11-1/sh-S100A11-2 exhibited the opposite results to that of pENTER-S100A11 on SiHa cells.ConclusionOverexpression of S100A11 promotes the proliferation, migration, invasion, and epithelial-mesenchymal transition of CC cells, and activates Wnt/β-catenin signaling.

This study aims to examine the expression of p53, p16, and murine double minute 2 (MDM2) protein in normal endometrium and endometriosis, in order to discuss the role of p53, p16, and MDM2 protein and apoptosis in the pathogenesis and development of endometriosis, and provide a theoretical basis for clinical diagnosis and treatment. The immunohistochemical streptavidin-biotin peroxidase method was used to detect the expression of p53, p16, and MDM2 in tissue samples obtained from 30 women with pathologically confirmed ovarian endometriosis and 29 women with pathologically confirmed normal endometrium. The relationship between p53, p16, and MDM2 expression and apoptosis was analyzed. In normal endometrium, the positive rate of p53 in the secretory phase was higher than that in the proliferative phase ( P < .05). Furthermore, the positive rate of p53 in normal endometrium was higher than that in ovarian endometriosis ( P < .05). There was a significant difference between normal endometrium and ovarian endometriosis. The positive rate of p16 in normal endometrium was higher than that in ovarian endometriosis ( P < .05). Furthermore, there was a significant difference between normal endometrium and ovarian endometriosis. The positive rate of MDM2 in normal endometrium was lower than that in ovarian endometriosis ( P < .05). In ovarian endometriosis, the expression of p53 and p16 was positively correlated with each other ( r = 0.611, P < .01). However, the expression of p53 and MDM2 was negatively correlated with each other ( r = −0.541, P < .01). Furthermore, the expression of p16 and MDM2 might not be relevant in the endometriosis ( r = 0.404, P > .05). As important apoptosis regulatory genes, p53, p16, and MDM2 might be involved in the pathogenesis and development of endometriosis.

Cervical cancer (CC) is one of the most common gynecological malignancies, and metastasis limits the use of surgical resection. Metapristone (MIF) was reported to suppress the proliferation and migration of several cancer cells. Exosomes play a variety of roles in cellular biological processes. The relation of exosomes and CC is less studied. Cell viability, apoptosis assay and migration assay was conducted in HeLa cells treated by MIF by CCK-8 kit, staining by Annexin V-fluorescein isothiocyanate and propidium iodide, and wound test respectively. ISG15 expression level was examined in MIF-treated HeLa cells by Western blot. The migration of HeLa cells treated by MIF/GW4869 was measured by wound test. MIF suppressed the growth and migration, as well as induced apoptosis of CC cells. MIF inhibited the exocrine secretion of CC cells by upregulating ISG15, while treating CC cells by ISG15 stimulus, IFN, inhibited the secretion of exosomes. The inhibition of exocrine secretion by GW4869 enhanced the migration inhibition of MIF on CC cells. This study demonstrates that MIF suppresses the CC cell migration by inhibiting exocrine secretion through upregulating ISG1.

This article was aimed to study the FOXF2 effects on cervical cancer. Tumor tissues and adjacent tissues of 41 cervical cancer patients were collected. Human endometrial epithelial cells (hEEC) and Hela cells were cultured. FOXF2 expression vector and its empty vector were transfected into Hela cells, and named as pcDNA 3.1-FOXF2 group and Vector group, respectively. Hela cells without any treatment were set as Blank group. qRT-PCR was used to detect mRNA expression. Nude mouse xenograft assay was performed to test Hela cells proliferation ability in vivo. FOXF2 and β-catenin positive cell numbers were detected by immunohistochemistry. Protein expression was analyzed by Western blot. Cells migration and invasion were conducted by Transwell. Tumor tissues and Hela cells FOXF2 expression were lower than that in adjacent tissues and hEEC (P<0.01). Low FOXF2 expression predicted poor outcomes of cervical cancer patients. Compared with Blank group and Vector group, Hela cells of pcDNA 3.1-FOXF2 group were with higher FOXF2 expression, lower OD495 value, migrated and invaded cells, higher E-cadherin expression, lower Vimentin and Snail expression, smaller tumor volume in nude mice, lower c-Myc, CyclinDl, MMP9, Lgr5, and nuclear β-catenin expression (all P<0.01). FOXF2 inhibits Hela cells proliferation, migration, and invasion through regulating Wnt signaling pathway.